Nitric oxide (NO) is a cell signaling molecule that acts as a neurotransmitter in the human brain. However, under neurodegenerative conditions, when the level of nitric oxide increases several folds of magnitude, various disease states can result. For instance, high levels of NO contribute to the damage of brain tissue, protein aggregation and degradation of the sort associated with various neurodegenerative disease states including but not limited to Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis (ALS), cerebral palsy and stroke/ischemic brain damage. By inhibiting the enzyme that produces NO in the brain, neuronal nitric oxide synthase (nNOS), neurodegeneration can be attenuated or prevented. However, most inhibitor compounds investigated to date are mimics of the natural substrate of nNOS, the amino acid L-arginine. Such compounds are basic and highly charged under physiological conditions, adversely affecting blood-brain barrier (BBB) permeation. In addition, designing useful nNOS inhibitors requires selectivity over two enzyme isoforms, inducible NOS (iNOS) and endothelial NOS (eNOS) to avoid unintended negative side effects. Accordingly, there remains an on-going concern in the art to develop new molecular scaffolds, with improved BBB permeability for selective nNOS inhibition.